The divorce between the BMA and real science is now
complete. The decline of modern medicine, as so cogently reported in James Le
Fanus remarkable book, has brought it to an impasse
in which it is reduced to admonitory quackery. The BMA has come out with a
report on Smoking and reproductive life, designed to hit the
headlines, which it did most successfully. It is a long document, available
on the web, and is nothing less than a celebratory festival of junk science.

Here are just a few quotations from it. Remember the
normal scientific standards for significance of relative risks
and watch out for the weasel words (our emphasis).

A growing body of evidence suggests that smoking may
cause male sexual impotence.Certain studiessuggest that smokers are at least 50 per cent more
likely to suffer from erectile dysfunction.It is estimated that in the UK, 120,000 men aged
3050 years are impotent because of smoking.The effect is seen in men of all ages.One study of almost 4,500 men aged 3149 years found
that in smokers, the risk of impotence was 1.5 times that in non-smokers.

Key messages:
Smoking and male sexual impotence

 Smoking may cause male sexual impotence.

 Smoking may amplify the effects of other
causes of sexual impotence.

 Stopping smoking appears to reduce the risk
of impotence and can improve sexual potency.

 There is limited evidence to suggest that
passive smoking may increase the risk of impotence.

Key messages:
Smoking and menstruation

 There is limited evidence that women who
smoke may be more likely to have painful periods orirregular periods.

 There is limited evidence to suggest that
smoking is associated with missed periods in women whohave previously menstruated.

The graph for the next bit shows that smokers on the
pill have a relative risk of 90. Oh yeah? Could they possibly have dropped a
percentage sign?

Key messages:
Smoking and oral contraceptives

 Smoking greatly increases the risk of heart disease
among women who use the combined oralcontraceptive pill. (See
here)

 Smoking may increase the risk of stroke
among women who use the combined oral contraceptive pill.

 There is evidence to suggest that smoking
may increase the risk of failure of the combined oral contraceptive pill.

They did not, of course, miss out the old sperm count
scam. It has been debunked frequently, but still comes up with monotonous
regularity (Search Junkscience.com)
The tenuous claim of a reduction in sperm counts has been ascribed by
epidemiologists, among other things, to GM foods, endocrine disrupters,
insecticides, dioxins, pollution, canned foods, dental sealants, certain
types of food, finger length, benzene, toiletries, disposable diapers, tight
jeans, low folic acid levels and of course:

Key messages:
Smoking and fertility

 Men who smoke have a lower sperm count and a higher
proportion of malformed sperm.

 Women who smoke take longer to conceive.

 Women who smoke are twice as likely to be infertile
as non-smokers.

 Men and women who smoke have a poorer response to
fertility treatment.

 Women who have stopped smoking take no longer to
become pregnant than women who have never smoked.

 Stopping smoking improves sperm count and quality.

Key messages:
Smoking during pregnancy

 Women who smoke are at increased risk of
ectopic pregnancy.

 Women who smoke during pregnancy may be at
increased risk of having a miscarriage.

 Women who smoke are three times more likely
to have a low birth-weight baby.

 Women who smoke during pregnancy are more likely
to suffer a stillbirth.

 Babies born to women who smoke during pregnancy are
more likely to die during the first fourweeks of life.

A
recent review of the evidence concluded that on average, infants born to women
exposed to second-hand smoke during pregnancy are 4050g lighter than
those born to women who are not exposed.

Note:
that is about one percent. Such precision!

Pregnant
women exposed to other peoples tobacco smoke are about 20 per cent
more likely to have a low birth-weight baby.

There is some evidence to suggest that women
who are exposed to second-hand smoke during their pregnancy
are at increased risk of giving birth prematurely.

One study found that mothers exposed daily to
second-hand smoke had a 23 per cent increased risk of giving birth
prematurely.

Cancer

There is limited evidence to suggest
that parental smoking may be linked to an increased risk of childhoodcancer.Smoking
by the father has been associated with an increased risk of lymphoma and
brain tumours,while maternal smoking has been linked to slightly increased risk for all
childhood cancer (relative risk 1.11)
and leukaemia (relative risk 1.14). While certain studies have reported that
children exposed to second-hand smoke during childhood have an increased risk of
cancer during adulthood, a recent evaluation judged the evidence to be
inconclusive.

What
they choose to ignore is that tobacco, like alcohol, is a great stress reliever.
Stress is a known cause of disease in people and animals. So:

Smoking rates across the country  both regional and
local  reflect socioeconomic trends. The greater the level of socioeconomic
deprivation, the higher the rate of smoking. Within England,smoking rates
are lowest in the South at around 24 per cent, but highest in London151 and the North,
at around 29 per cent. In Scotland,smoking rates have been found to vary between postcode
areas from 15 per cent to 71 per cent. Rates of smoking among the most
disadvantaged are extremely high. A lone mother with a poor level of education,
living in council accommodation and receiving income support has an 80 per cent
risk of being a smoker.

But
of all thetrashy science in this tawdry document, it is the appendix that is truly


Outrageous!

Appendix A:
Assessment of causality

Assessment
of the relationship between and exposure and a particular outcome is made on the
balance of all the available evidence. Sir Austin Bradford-Hill proposed several
considerations to be taken into account, which have been widely used and
adapted. Some key considerations follow.

Strength of the association

Strong associations are more likely to be
causal than weak ones. Weak associations are more likely to be explained by
undetected biases. However, this does not rule out the possibility of a weakassociation being causal.

Consistency of the association

An association is more likely to be causal
when a number of similar results emerge from different studies done in different
populations. Lack of consistency, however, does not rule out a causal
association.

Temporality

For an exposure to cause an outcome, it
must precede the effect.

Plausibility

Is there a biologically plausible mechanism
by which the exposure could cause the outcome? The existence of a plausible
mechanism may strengthen the evidence for causality; however, lack of such a mechanism may simply reflect
limitations in the current state of knowledge.

Biological gradient

The observation that an increasing dose of
an exposure increases the risk of an outcome strengthens theevidence for causality. Again, however,
absence of a dose-response, does not rule out a causal association.

Coherence

Coherence implies that the association does
not conflict with current knowledge about the outcome.

Experimental evidence

Experimental studies in which changing the
level of an exposure is found to change the risk of an outcome provide strong
evidence for causality. Such studies may not, however, always be possible,
for practical or ethical reasons.

Any woman who takes any drug while
pregnant is guilty of inflicting it on another innocent individual,
unforgivable, but that does not justify this arrogant, mendacious, tract of
unscientific rubbish. The emphasised words are all additions to the great man's
rules that actually completely reverse their meaning. The defilement of Hill's
precepts, mainly by use of the logical fallacy argumentum ad ignorantiam,
is an unprecedented disgrace, which in a just world would result in the authors
being drummed out of their profession.